6572 Acute Adrenal Crisis Secondary To Undiagnosed Addison's Disease

Abstract Disclosure: J.M. Deirmenjian: None. H. Nickowitz: None. T. Kavafyan: None. Addison’s disease, also known as primary adrenal insufficiency, is when the adrenal gland has a defect in making cortisol. Signs and symptoms of Addison’s disease include nausea, vomiting, diarrhea, fatigue, dizziness, hyperpigmentation, and mood changes. Acute Adrenal Crisis can occur as a result of Addison’s disease when patients experience acute physiologic stress such as acute illness. Patient is a 35- year-old woman with a PMHx of iron deficiency anemia presenting with intractable nausea and vomiting for 10 days and a single witnessed syncopal episode two days prior to presentation. She was also had intermittent dizziness. Patient initially presented to urgent care where she was found to be hyponatremic and then was sent to the ED. She had no seizure like activity or rashes prior to admission. On initial physical exam, her skin was warm and dry with skin discoloration and hyperpigmentation. She was awake, alert, and oriented to person, place, time, and situation. Patient had no neurological deficits and no lateral or vertical nystagmus on initial assessment. On admission, patient was hyponatremic to 114 mEq/L, potassium was 5.0 mEq/L, and glucose level was 79 mg/dL. Despite receiving a 500 cc NS bolus, 1L NS bolus, 25 grams of albumin, and D5-0.45 NS at 50 cc/hr, the hyponatremia was difficult to correct. Her sodium initially corrected to 120 mEq/L but the sodium later decreased to 117 mEq/L. The morning after admission, patient became hypotensive and hypoglycemic. Random cortisol was measured and found to be 2.2 mcg/dL, raising concern for acute adrenal crisis as a result of undiagnosed Addison’s Disease. ACTH level was 17 pg/mL. Endocrinology was consulted and she was treated with IV 100 mg Hydrocortisone in addition to IV hydrocortisone 50 mg IV q6h. Patient was able to be transitioned to PO hydrocortisone 15 mg qAM and 5 mg qPM and was started on PO fludrocortisone 0.1 mg daily. On day of discharge, sodium improved to 127 mEq/L. CT Abdomen with contrast was completed to evaluate the adrenal glands and it showed a normal appearance of the adrenal glands. The etiology of the patient’s acute adrenal crisis was secondary to undiagnosed Addison’s Disease. It is interesting to note that patient was not hypoglycemic on admission but later became hypoglycemic during her hospital course. Adrenal crisis is a possible fatal complication of undiagnosed Addison’s disease. Therefore, a possible Addison’s Disease diagnosis is important to consider when patients are presenting with symptoms such as nausea, vomiting, dizziness, and electrolyte derangements including hyponatremia. If patient’s present with hyponatremia, ruling out possible adrenal insufficiency by checking a cortisol level may change the course of patient’s care. After discharge, she was able to establish care with Endocrinology and remain stable on treatment with PO hydrocortisone and PO fludrocortisone. Presentation: 6/3/2024